The arterial baroreceptors play a major role in the regulation of sympathetic activity and of arterial blood pressure in acute cardiovascular stresses such as hemorrhage and in pathophysiologic states such as hypertension. Activation of the arterial baroreceptors during a rise in arterial pressure provokes a reflex inhibition of sympathetic activity and a buffering of the rise in arterial pressure. The level of arterial pressure at which these receptors will fire and the sensitivity of their activation by the rise in pressure is therefore an important determinant of the neural regulation of arterial pressure. For example, in hypertensive states, these baroreceptors are "reset" so that they fire at a higher pressure and their sensitivity is reduced, contributing to the sustained elevation of arterial pressure. This phenomenon of resetting may be demonstrated with temporary elevations of arterial pressure over a period of 10-15 minutes (acute resetting). The purpose of these studies is to examine: 1) the basic mechanisms involved in the phenomenon of acute resetting of arterial baroreceptors: specifically, the contribution of changes in mechanical (viscoelastic) properties of the carotid sinus region to baroreceptor resetting versus the contribution of possible changes in the receptor membrane; (2) the influence of the resetting on efferent sympathetic activity and the possible role of "central resetting" versus the peripheral resetting which is known to occur at the level of the baroreceptor; and 3) the potential importance of "acute resetting" in the reflex control in hypertensive animals. In order to assess the mechanism(s) of peripheral resetting, both multifiber and single unit afferent carotid baroreceptor discharge will be recorded during treatments that produce or attenuate the resetting process. Diameter of the carotid sinus will be measured simultaneous with baroreceptor discharge in some experiments. Central mechanisms will be examined by manipulating the central afferent input (stimulation of afferent nerves) and observing the effects on reflex control of efferent sympathetic nerve activity. "Acute resetting" in hypertensive and normotensive rabbits will be compared and the mechanisms explored. These studies will clarify the role of an important phenomenon in reflex neurogenic control of the circulation and permit examination of the basic mechanisms involved in this phenomenon in physiologic and pathophysiologic states.